Frozen Shoulder

Frozen Shoulder (Adhesive Capsulitis)

Frozen Shoulder: An Introduction

Frozen shoulder, medically termed Adhesive Capsulitis, is a painful and disabling condition of the shoulder joint characterized by stiffness, restricted range of motion, and pain. It is a common musculoskeletal disorder seen particularly in individuals between the ages of 40 and 60 years, with a higher prevalence in women than men. Both modern medicine and Ayurveda describe frozen shoulder in different perspectives — pathology, causative factors, stages, and management.

Anatomy & Physiology of the Shoulder Joint

The shoulder joint (glenohumeral joint) is a ball-and-socket joint, allowing a wide range of movements such as abduction, flexion, extension, rotation, and circumduction. It is stabilized by:

Joint capsule (encloses the joint)

Ligaments and tendons (especially rotator cuff tendons)

Synovial fluid (lubricates the joint)

In frozen shoulder, the capsule becomes thickened, inflamed, and contracted, leading to pain and limited mobility. Adhesions (fibrous bands) form inside the capsule, restricting movements further.

Causes & Risk Factors

Modern Perspective

Idiopathic (primary): No clear cause.

Secondary causes:

Diabetes mellitus (most common association)

Thyroid disorders (hypothyroidism, hyperthyroidism)

After prolonged immobilization (fracture, surgery, stroke)

Cervical spondylosis or cardiac conditions

Trauma or injury to the shoulder

Risk factors:

Age (40–60 years)

Female gender

Systemic diseases (DM, thyroid disorders, Parkinson’s disease)

Pathophysiology

Inflammation of the synovium and capsule

Fibrosis and thickening of the capsule

Adhesion formation inside capsule

Progressive restriction of shoulder movement

Clinical Features

Gradual onset of shoulder pain, worse at night

Stiffness and restriction of both active & passive movements

Pain on external rotation is most significant

Difficulty in daily activities: combing hair, wearing clothes, reaching objects

Stages of Frozen Shoulder (Modern Medicine)

Freezing stage (Painful phase):

Lasts 2–9 months

Pain predominates, stiffness gradually develops

Frozen stage (Stiffness phase):

Lasts 4–12 months

Pain reduces, but severe restriction of movement

Thawing stage (Recovery phase):

Lasts 6–24 months

Gradual return of movement, function improves

Diagnosis

Clinical examination: Restricted passive and active movement, especially external rotation.

Imaging:

X-ray (to rule out arthritis, fracture, calcification)

MRI / Ultrasound (to assess capsule thickening, rotator cuff injury)

Management

Modern Medical Approach

Conservative treatment:

Pain management with NSAIDs, corticosteroid injections

Physiotherapy & stretching exercises

Advanced treatment:

Hydrodilatation (capsular distension)

Manipulation under anesthesia (MUA)

Arthroscopic capsular release (in resistant cases)

Physiotherapy Exercises

Pendulum exercises

Wall climbing

Towel stretching

External rotation with stick

Isometric strengthening

Ayurvedic Perspective

Correlation

In Ayurveda, Frozen Shoulder can be correlated with Avabahuka, described by Acharya Sushruta under Vata Nanatmaja Vyadhi (diseases caused purely by vitiated Vata).

Dosha involvement: Predominantly Vata dosha (dryness, stiffness) and Kapha dosha (heaviness, obstruction).

Dushya: Snayu (ligaments), Sandhi (joints), Mamsa (muscles).

Samprapti (pathogenesis): Vitiated Vata leads to Sankocha (constriction), Stambha (stiffness), and Shoola (pain) in the shoulder joint.

Ayurvedic Symptoms of Avabahuka

Bahu shoola (shoulder pain)

Bahu stambha (stiffness)

Bahu sankocha (restricted movements)

Ayurvedic Treatment

Shodhana Chikitsa (Detoxification)

Snehana (Oleation): Local application and internal use of medicated oils (Maha Narayan Taila, Dhanwantaram Taila).

Swedana (Sudation): Nadi sweda, Patra Pinda Sweda, Valuka Sweda to reduce stiffness.

Basti Chikitsa (Medicated enema): Matra Basti with Dashamoola taila or Eranda taila – best for Vata disorders.

Shamana Chikitsa (Palliative)

Oral medicines:

Rasnasaptaka kwatha

Dashamoola kwatha

Yogaraja Guggulu

Simhanada Guggulu

Lakshadi Guggulu

Medicated oils: Maha Narayan Taila, Sahacharadi Taila, Ksheerabala Taila

Panchakarma Procedures

Abhyanga (oil massage)

Pizhichil (oil bath)

Shirodhara (relaxation of nervous system)

Patra pinda sweda (bolus fomentation with medicated leaves)

Basti karma (enema – most effective for chronic cases)

Yoga & Lifestyle

Yoga postures: Tadasana, Gomukhasana, Bhujangasana, Dhanurasana (gentle stretching under guidance).

Pranayama: Anulom-Vilom, Bhramari for stress relief.

Avoid cold exposure, heavy lifting, and irregular lifestyle which aggravate Vata.

Prognosis

Self-limiting condition, but may take 1–3 years for complete recovery.

Early intervention with physiotherapy or Ayurveda therapies shortens duration and prevents disability.

In diabetic patients, prognosis is relatively slower.

Preventive Measures

Regular shoulder mobility exercises

Avoid prolonged immobilization after injury/surgery

Maintain blood sugar levels in diabetic patients

Balanced lifestyle and Vata-pacifying diet in Ayurveda (warm, unctuous, nourishing foods)

Conclusion

Frozen shoulder (Adhesive Capsulitis / Avabahuka) is a common but disabling condition of the shoulder joint. It progresses through phases of pain, stiffness, and gradual recovery. Modern medicine emphasizes physiotherapy, analgesics, and surgical options in resistant cases, while Ayurveda provides holistic management through Panchakarma, herbal formulations, and lifestyle modifications. A combined approach ensures faster recovery, functional improvement, and prevention of recurrence.

Anatomy of Shoulder Joint

The shoulder joint is one of the most mobile and complex joints in the human body. It provides a wide range of motion, allowing us to perform daily activities like lifting, throwing, pushing, pulling, and rotating the arm. At the same time, this mobility makes the shoulder joint relatively unstable, requiring the support of ligaments, tendons, and muscles for stability. Below is a comprehensive overview of the anatomy of the shoulder joint.

Type of Joint

The shoulder joint (glenohumeral joint) is a synovial ball-and-socket joint.

It is formed between the head of the humerus (ball) and the glenoid cavity of the scapula (socket).

The socket is shallow compared to the hip joint, giving greater mobility but less stability.

Bones Involved

Humerus

The upper arm bone, with a rounded head that fits into the glenoid cavity.

Scapula (Shoulder blade)

The glenoid cavity forms the socket for articulation.

The scapula also provides attachment for several muscles.

Clavicle (Collar bone)

Connects the shoulder girdle to the axial skeleton.

Forms the acromioclavicular (AC) joint and the sternoclavicular joint, which help in shoulder movement.

Articular Surfaces

Head of humerus – spherical, smooth, and covered with hyaline cartilage.

Glenoid cavity of scapula – shallow and pear-shaped, also lined with cartilage.

Glenoid labrum – fibrocartilaginous rim around the glenoid cavity that deepens the socket and provides extra stability.

Capsule and Ligaments

Joint Capsule

A thin, loose fibrous capsule attached around the margins of the glenoid cavity and the anatomical neck of the humerus.

Allows free movement but needs reinforcement.

Ligaments (extracapsular and intracapsular)

Glenohumeral ligaments (superior, middle, inferior) – strengthen the anterior part of the capsule.

Coracohumeral ligament – extends from the coracoid process to the humerus; prevents downward dislocation.

Transverse humeral ligament – holds the tendon of the long head of the biceps in the bicipital groove.

Coracoacromial ligament – forms an arch above the joint preventing upward dislocation.

Muscles Supporting the Shoulder

The Rotator Cuff Muscles play a key role in stabilizing the joint:

Supraspinatus – initiates abduction.

Infraspinatus – external rotation.

Teres minor – external rotation.

Subscapularis – internal rotation.

Other important muscles:

Deltoid – main abductor of the arm.

Pectoralis major, Latissimus dorsi, Teres major – adduction and medial rotation.

Trapezius, Serratus anterior, Levator scapulae, Rhomboids – control scapular movement and contribute indirectly to shoulder stability.

Bursae of the Shoulder

Subacromial bursa – reduces friction between acromion and supraspinatus tendon.

Subdeltoid bursa – between deltoid muscle and joint capsule.

Subscapular bursa – communicates with the joint cavity.

These bursae act as cushions to prevent friction and inflammation.

Nerve Supply

Derived mainly from the brachial plexus:

Suprascapular nerve

Axillary nerve

Lateral pectoral nerve

According to Hilton’s law, the nerves supplying the joint also supply the muscles acting on it and the skin covering it.

Blood Supply

Rich vascular supply from:

Anterior and posterior circumflex humeral arteries

Suprascapular artery

Scapular circumflex artery

Movements of the Shoulder Joint

The shoulder joint allows the widest range of movements in the human body:

Flexion & Extension – Forward and backward movement.

Abduction & Adduction – Moving the arm away from or towards the body.

Medial (Internal) & Lateral (External) Rotation.

Circumduction – A combination of all movements in a circular manner.

Applied Anatomy (Clinical Aspects)

Dislocation – Most common joint to dislocate (anterior dislocation most frequent).

Rotator cuff injuries – Common in athletes (e.g., baseball pitchers, swimmers).

Frozen shoulder (Adhesive capsulitis) – Stiffness and pain due to capsule thickening.

Bursitis – Inflammation of bursae, often subacromial bursitis.

Arthritis – Osteoarthritis or rheumatoid arthritis can affect the joint.

Conclusion

The shoulder joint is a highly mobile but relatively unstable joint. Its stability depends not only on the bony architecture but also on the surrounding capsule, ligaments, rotator cuff muscles, and bursae. Understanding its anatomy is essential for diagnosing and managing common shoulder injuries and disorder.

Muscle Attachment in the Shoulder Joint

The shoulder joint (glenohumeral joint) together with the scapulothoracic articulation forms the shoulder complex. Its stability and wide range of motion are primarily maintained by muscular attachments. These include the rotator cuff, deltoid, scapular stabilizers, and other large thoraco-humeral muscles. Below is a comprehensive description of all major muscles: their origin, insertion, innervation, action, and clinical significance.

Rotator Cuff (SITS muscles)

Role: Dynamic stabilizers; compress humeral head into the glenoid fossa, preventing dislocation during movement.

Supraspinatus

Origin: Supraspinous fossa of scapula

Insertion: Greater tubercle of humerus (superior facet)

Nerve: Suprascapular nerve (C5–C6)

Action: Initiates abduction (first 15°), stabilizes humeral head

Infraspinatus

Origin: Infraspinous fossa

Insertion: Greater tubercle (middle facet)

Nerve: Suprascapular nerve (C5–C6)

Action: External rotation, posterior stabilization

Teres Minor

Origin: Lateral border of scapula (upper 2/3)

Insertion: Greater tubercle (inferior facet)

Nerve: Axillary nerve (C5–C6)

Action: External rotation, inferior-posterior stabilization

Subscapularis

Origin: Subscapular fossa (anterior scapula)

Insertion: Lesser tubercle of humerus

Nerve: Upper & Lower subscapular nerves (C5–C7)

Action: Internal rotation, anterior stabilization

Deltoid – Primary Abductor

Origin: Lateral 1/3 clavicle (anterior), acromion (middle), scapular spine (posterior)

Insertion: Deltoid tuberosity of humerus

Nerve: Axillary nerve (C5–C6)

Action:

Anterior fibers: Flexion, internal rotation

Middle fibers: Abduction (15°–90°)

Posterior fibers: Extension, external rotation

Scapulohumeral (Intrinsic) Muscles

Teres Major

Origin: Inferior angle of scapula (posterior)

Insertion: Medial lip of intertubercular sulcus of humerus

Nerve: Lower subscapular nerve (C5–C7)

Action: Adduction, extension, internal rotation (“Lat’s little helper”)

Coracobrachialis

Origin: Coracoid process of scapula

Insertion: Medial shaft of humerus (mid-point)

Nerve: Musculocutaneous nerve (C5–C7)

Action: Flexion, adduction, resists downward dislocation

Thoraco-humeral (Extrinsic) Muscles

Latissimus Dorsi

Origin: T7–L5 spinous processes, thoracolumbar fascia, iliac crest, ribs 9–12

Insertion: Floor of intertubercular sulcus of humerus

Nerve: Thoracodorsal nerve (C6–C8)

Action: Extension, adduction, internal rotation

Pectoralis Major

Origin: Medial clavicle (clavicular head), sternum and costal cartilages (sternocostal head)

Insertion: Lateral lip of intertubercular groove

Nerve: Lateral and medial pectoral nerves (C5–T1)

Action: Adduction, internal rotation, flexion (clavicular head), extension from flexed position (sternal head)

Scapular Stabilizers

Maintain scapulothoracic rhythm (2:1 ratio with GH movement).

Trapezius

Origin: Occiput, nuchal ligament, C7–T12 spinous processes

Insertion: Lateral clavicle, acromion, scapular spine

Nerve: Spinal accessory (CN XI) + C3–C4 (sensory)

Action: Upper—elevation/upward rotation; Middle—retraction; Lower—depression/upward rotation

Serratus Anterior

Origin: Ribs 1–8/9

Insertion: Anterior medial border of scapula

Nerve: Long thoracic nerve (C5–C7)

Action: Protraction, upward rotation, prevents winging

Rhomboids (Major & Minor)

Origin: C7–T1 (minor), T2–T5 (major)

Insertion: Medial border of scapula

Nerve: Dorsal scapular nerve (C4–C5)

Action: Retraction, downward rotation

Levator Scapulae

Origin: C1–C4 transverse processes

Insertion: Superior medial border of scapula

Nerve: Dorsal scapular (C5) + C3–C4

Action: Elevation, downward rotation

Additional Muscles Involved

Biceps Brachii (long head stabilizes GH joint)

Origin: Supraglenoid tubercle (long head), coracoid (short head)

Insertion: Radial tuberosity & aponeurosis

Nerve: Musculocutaneous (C5–C6)

Action: Elbow flexion, supination, GH stability

Triceps (Long head)

Origin: Infraglenoid tubercle

Insertion: Olecranon process (ulna)

Nerve: Radial nerve (C6–C8)

Action: Elbow extension, assists GH extension/adduction

Pectoralis Minor

Origin: Ribs 3–5

Insertion: Coracoid process

Nerve: Medial pectoral nerve (C8–T1)

Action: Anterior tilt, protraction of scapula

Functional Groups of Muscles

Centralizers (stabilizers): Rotator cuff + long head of biceps

Power movers: Deltoid, pectoralis major, latissimus dorsi, teres major

Upward rotators: Serratus anterior, trapezius (upper & lower)

Downward rotators: Rhomboids, levator scapulae, pectoralis minor

External rotators: Infraspinatus, teres minor, posterior deltoid

Internal rotators: Subscapularis, latissimus dorsi, pectoralis major, teres major, anterior deltoid

Abductors: Supraspinatus (initiation), deltoid (prime mover)

Adductors/Extensors: Latissimus dorsi, teres major, pectoralis major (sternal), triceps long head

Clinical Significance of Muscle Attachments

Supraspinatus tendon: Common site of impingement and tears (poor blood supply)

Infraspinatus/Teres minor: Injured in overhead throwing athletes

Subscapularis: Tears cause loss of internal rotation, instability of biceps tendon

Biceps long head: SLAP lesions (labral tears), tendinitis

Serratus anterior weakness: Winging of scapula (long thoracic nerve palsy)

Axillary nerve injury: Deltoid and teres minor weakness, flattened shoulder contour

Myotomes (Nerve Roots)

C5: Supraspinatus, deltoid (abduction)

C6: Biceps, infraspinatus (external rotation)

C7–C8: Latissimus dorsi, pectoralis major (sternal), triceps long head

C5–C7: Subscapularis, teres major, serratus anterior

Mnemonics for Easy Recall

Rotator cuff (SITS): Supraspinatus, Infraspinatus, Teres minor, Subscapularis

Greater tubercle facets (Top–Middle–Bottom): Supra–Infra–Teres minor

Bicipital groove (L-T-P): Latissimus dorsi (floor), Teres major (medial lip), Pectoralis major (lateral lip)

In summary, the shoulder joint muscle attachments provide the delicate balance between stability (by rotator cuff and scapular stabilizers) and mobility (by large movers like deltoid, latissimus dorsi, and pectoralis major). Understanding these attachments is essential for anatomy, biomechanics, clinical examination, and rehabilitation.

Here’s a comprehensive, clinician-level overview of the pathogenesis of frozen shoulder (adhesive capsulitis)—from triggers to tissue-level biology, anatomic sites of disease, and how these changes create the classic clinical course.

What is “frozen shoulder” pathologically?

Frozen shoulder is a self-limited fibro-inflammatory disorder of the glenohumeral joint characterized by:

Early synovitis (painful inflammatory phase),

Progressing to capsular fibroplasia and contracture (stiff phase),

Eventual slow remodeling (thawing).

It primarily involves the joint capsule and rotator interval (including the coracohumeral ligament), with secondary effects on periarticular structures.

Etiological framework: primary vs secondary

Primary (idiopathic)

No clear inciting event; strong association with metabolic–endocrine disorders (notably diabetes mellitus) and sometimes thyroid disease.

Thought to arise from a dysregulated local immune and fibrotic response in a susceptible host.

Secondary

Intrinsic shoulder pathology: rotator cuff disease/tears, biceps tendinopathy, calcific tendinitis.

Extrinsic factors: prolonged immobilization after trauma/surgery, cervical radiculopathy, cardiothoracic procedures, breast surgery/radiation.

Systemic factors: diabetes, prediabetes/insulin resistance, thyroid dysfunction, dyslipidemia, autoimmune tendencies.

Key risk amplifiers: age 40–65, female sex, prior episode in the opposite shoulder, and prolonged immobilization.

The three-phase clinical course mapped to biology

Freezing (painful inflammatory) phase

Dominant process: active synovitis of the capsule (especially anterosuperior capsule and rotator interval).

Cellular milieu: macrophages, T cells, mast cells, and proliferating fibroblasts/myofibroblasts; neo-angiogenesis and neurogenic inflammation (substance P, CGRP) increase nociception.

Symptoms: severe night pain, escalating pain with end-range stretch; ROM loss begins.

Frozen (stiff) phase

Shift to fibrosis: synovial lining attenuates while dense collagen deposition and myofibroblast-driven contraction thicken and shorten the capsule.

Biomechanical result: marked loss of capsular compliance; external rotation most restricted (tight coracohumeral ligament/rotator interval), then abduction and internal rotation.

Thawing (remodeling) phase

Slow matrix turnover and partial resolution of myofibroblasts permit gradual recovery of ROM; pain subsides first, stiffness resolves later.

Tissue-level pathobiology

Inflammation → Fibrosis continuum

Cytokines/growth factors: IL-1β, IL-6, TNF-α (inflammatory drive); TGF-β, PDGF, CTGF (fibrogenic switch).

Matrix remodeling imbalance: ↓MMP activity and ↑TIMPs favor extracellular matrix accumulation (types I and III collagen).

Myofibroblast phenotype: fibroblasts acquire α-SMA expression, generate contractile force, and lay down aligned collagen → capsular shrinkage/contracture.

Neurogenic inflammation & pain sensitization

Increased local neuropeptides (substance P, CGRP) and nerve ingrowth around vessels support peripheral sensitization.

Central sensitization can evolve with persistent nociception, explaining disproportionate pain early in disease.

Microvascular & hypoxic influences

Neovascularization with fragile vessels and relative tissue hypoxia promote fibrogenic signaling (via HIF-1 pathways) and perpetuate myofibroblast activity.

Metabolic–endocrine modifiers (why diabetes matters)

Advanced glycation end products (AGEs) create irreversible collagen cross-links, stiffening the capsule and resisting enzymatic degradation.

Hyperglycemia and insulin resistance enhance TGF-β signaling, tilt MMP/TIMP balance, and may blunt normal remodeling—raising risk, severity, and chronicity.

Anatomic pattern of disease

Rotator interval & coracohumeral ligament (CHL): hallmark thickening/contracture → loss of external rotation.

Anterior–inferior capsule & axillary recess: fibrosis/adhesions → loss of abduction and elevation; axillary pouch often obliterated.

Subscapularis recess & biceps pulley: synovitis and scarring may limit internal rotation and cause bicipital pain.

Posterior capsule: variably involved, often later, contributing to cross-body adduction pain.

Imaging correlations (typical): thickened CHL and rotator interval on US/MRI, capsular thickening at the axillary recess, reduced capsular volume on arthrography; edema/enhancement in early phase, low-signal fibrotic bands in later phases.

Biomechanics of stiffness

Capsular contracture reduces the physiologic capsular “redundancy,” especially in the axillary pouch.

Loss of capsular glides (anterior/inferior) blocks concave–convex arthrokinematics during elevation and rotation.

Scapulothoracic compensation increases (early scapular upward rotation/protraction), but can’t restore end-range glenohumeral motion, producing the classic firm, painful end-feel.

Histopathology (what biopsies show)

Early: hypervascular synovitis with lymphocytes, mast cells, and proliferating fibroblasts.

Established: dense, haphazard collagen with myofibroblasts, reduced synovial lining cells—Dupuytren-like fibromatosis pattern.

Molecular signature: upregulated TGF-β/Smad pathway, elevated TIMP-1, decreased collagen-degrading MMPs.

Why it hurts first and stiffens later (the “switch”)

Pain-dominant phase: inflammatory mediators and neuropeptides sensitize nociceptors; mechanical stretch of an inflamed capsule is exquisitely painful.

Stiffness-dominant phase: as collagen matures and myofibroblasts contract the matrix, mechanical block supersedes inflammation; pain lessens at rest but persists at end-range due to capsular tension.

Integrated pathogenesis flow (cause → consequence)

Host susceptibility (age 40–65, female, diabetes/thyroid issues, prior episode)
→ Trigger (often minor injury, surgery, immobilization, or none recognizable)
→ Synovial inflammation (IL-1/IL-6/TNF-α; neurogenic peptides)
→ Fibrogenic switch (TGF-β/PDGF/CTGF; ↓MMP/↑TIMP)
→ Myofibroblast contraction + collagen deposition
→ Selective capsular thickening (rotator interval/CHL, anterior–inferior capsule)
→ Capsular volume loss & adhesions (axillary recess)
→ ROM loss pattern (ER → ABD → IR) with characteristic pain and stiffness
→ Gradual remodeling (matrix turnover) → partial/complete recovery over months.

Clinical implications (why pathogenesis matters for care)

Early phase (inflammation dominant): best window for analgesia/anti-inflammatory strategies, intra-articular corticosteroid, gentle pain-limited mobilization; aim to curb the fibrotic switch.

Established fibrosis: emphasize capsular stretch and graded mobilizations; hydrodilatation or MUA/arthroscopic capsular release target the CHL/rotator interval and anterior–inferior capsule, i.e., the actual sites of contracture.

Metabolic optimization: glycemic control may reduce severity/recurrence by moderating pro-fibrotic signaling.

Patient education: pain typically precedes stiffness; recovery is slow but expected as remodeling ensues.

One-paragraph takeaway

Frozen shoulder is not “adhesive” because of a single sheet of scar, but because an immune-mediated synovitis transitions into a myofibroblast-driven capsular contracture, especially in the rotator interval/coracohumeral ligament and anterior–inferior capsule. Metabolic factors (notably diabetes) amplify fibrogenesis via AGEs and TGF-β signaling. The disease thus hurts first (neuro-inflammatory), then stiffens (fibrotic contracture), and finally thaws (remodeling)—a sequence that explains both the clinical course and treatment logic.

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